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One of the most important articles is, “Update on the Prostate,” which you can find at: http://www.virginiahopkinstestkits.com/prostateupdate.html You can also find current articles on my blog, at http://www.virginiahopkinshealthwatch.com, including “5 ways men can reduce estrogen levels,” and “Muscle loss and testosterone in older men.”
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Inhibiting this conversion of testosterone to DHT is often a treatment goal for men with BPH. While there are pharmaceutical drugs to inhibit 5-alpha-reductase (e.g., Proscar, finisteride), it is better to use saw palmetto berry extract or progesterone, both of which inhibit 5 alphareductase and are safer than the pharmaceutical drugs.
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—Saw Palmetto berry extract: Studies indicate that it inhibits 5-alpha-reductase and it may block DHT from binding to prostatic androgen receptors; reduces prostatic edema (swelling), inhibits estradiol and antagonizes alpha-adrenergic receptors. —Nettle root: May inhibit aromatase, reducing conversion of androgens to estrogen. —Antioxidants, such as vitamin E, lycopene (found in cooked tomatoes), and vitamin C. —Polyphenols (e.g., catechins, found in green tea.) —Ellagic acid (found in nuts and raspberries) may trigger beneficial apoptosis. —Zinc (low zinc levels correlate with increased prostate disease). Be sure to get extra copper if you’re taking zinc for longer than a few weeks.
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Editorialist Peter T. Scardino, M.D., speculates that finasteride, in reducing prostate hyperplasia, might reduce PSA levels, thus delaying diagnosis. Thus, finasteride is not recommended for prevention of prostate cancer.
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Prostate cancer occurs because testosterone and progesterone levels fall with age and estradiol levels rise, leading to estrogen dominance in older men. The same mechanism that causes breast and endometrial cancer in women causes prostate cancer in men. It is time to set finasteride aside and turn to proper hormone balancing in men as well as in women.
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The Underlying Metabolic Imbalances that Lead to Prostate Cancer GENERAL —Metabolic acidosis —Trans-fatty acids —Lack of essential Omega-3 fatty acids —Excessive exposure to toxins —Insufficient daytime sun exposure = Vitamin D deficiency and mitochondrial inhibition —Thyroid deficiency may underlie many other deficiencies and oxidative damages SPECIFIC TO PROSTATE CANCER —Estrogen dominance —Testosterone deficiency —Use it or lose it (regular sexual activity is thought to be helpful) —Zinc deficiency —Insufficient nighttime sleep = Melatonin deficiency → Estrogen dominance
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left untreated, prostate cancer tends to eventually metastasize to bones.
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In women, the important factor is the ratio between progesterone (P) and estradiol (E2) when measured by saliva testing. A healthy P/E2 ratio in women is 200 to 300 to 1. Cancer of the breast and/or in the uterus most often occurs in women with a P/E2 ratio of less than 200 to 1. According to Dr. David Zava of ZRT, who has amassed a database of tens of thousands of saliva samples and questionnaires, these cancers occur very rarely in women with a healthy P/E2 ratio.
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In men, estrogen gradually rises with age, while saliva levels of progesterone and testosterone gradually fall with age. Thus, with aging, estrogen dominance occurs. Estrogen levels are particularly apt to increase in aging men who are overweight because fat cells convert testosterone and androstenedione into estrogens, which then stimulates prostate growth.
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Some research indicates that BPH and prostate cancer correlate with higher levels of sex hormone binding globulin (SHBG). As a result, some have hypothesized that SHBG may play a role in the cause of BPH and of prostate cancer. SHBG is the binding hormone for estradiol. Excessive levels of estradiol activate the liver to make more SHBG. Thus, it is likely that the elevated SHBG is merely a marker for excessive estradiol. Testosterone binds to both SHBG and simple albumin. It is like a hitchhiker who doesn’t care whether he catches a ride with a cattle car or rides the rails. The albumin binding is less secure, however, and the testosterone is more likely to become “free” of it. Therefore, serum (or plasma) levels of testosterone tend to run somewhat more parallel to saliva levels than, say, serum and saliva levels of progesterone. However, the only sure method of measuring “free” testosterone is saliva testing.
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As far as nutrition goes, the formation of this destructive metabolite of estradiol and estrone, as found by Dr. Cavalieri, is found most often in people who eat more trans fatty acids (e.g. hydrogenated oils), fewer of the “good” fats (e.g. olive oil, fish oil), and less of the sulfur-containing amino acids (beans, garlic, onions, broccoli, cauliflower, cabbage).
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Stress increases cortisol levels, which will make the body somewhat resistant to using its other hormones, and also increases oxidation, which is at the heart of how the DNA damage is caused by these estrogen metabolites.
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Estrogen dominance activates the oncogene Bcl-2, whereas progesterone and testosterone activate the protector gene, p53. In laboratory cultures of breast cancer cells, endometrial cancer cells, and prostate cancer cells, their proliferation is increased by Bcl-2, and prevented by p53. The same mechanism applies to all these types of cancer.
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The truth is that progesterone receptors are made by estrogen. The higher the estradiol/progesterone ratio, the greater are the number of progesterone receptors that will emerge. This is the tissue’s effort to restore proper progesterone function in situations where estrogen dominance is present. Thus, increase of progesterone receptors is evidence of estrogen dominance, and not evidence that progesterone increases the risk of cancer. There are also some theories that estrogen and testosterone hit the same receptors in the hypothalamus, the area of the brain that regulates hormone level feedback mechanisms. Thus, when estrogen levels are high, the brain may be getting the message that testosterone is high, and actually reducing testosterone production by the testes.
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Estrogen dominance has many causes but several are more common than others. In men they include insulin resistance, stress, and early (especially embryonic, during early life in the womb) exposure to petrochemical toxins (called xenoestrogens) such as pesticides, emulsifiers, and toxic chemicals that out-gas from certain plastics and adhesives (such as carpeting) that are common in the environment.
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Progesterone helps by restoring normal inhibition of 5-alpha-reductase, thus preventing testosterone from changing into dihydrotestosterone (DHT), which stimulates proliferation of prostate cells. Progesterone not only stimulates the action of the cancer-preventive gene, p53, but also maintains testosterone, which is a direct antagonist of estradiol.
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Causes of Estrogen Dominance The following factors may directly or indirectly cause or contribute to estrogen dominance: —Insulin resistance and obesity (brought about by excess sugars and refined starches) —Trans fatty acids (as in pastries and highly processed foods) —Chronic stress (excess cortisol) —Sleep deprivation —Working nights under bright lights and trying to sleep in the daytime (the melatonin effect) —Fluoridated water and toothpaste —Environmental xenoestrogens —Cigarette smoking —Zinc deficiency —Testosterone deficiency —Progesterone deficiency —Sedentary life style —Cadmium toxicity —Lack of sulfur-containing amino acids and glutamine —Lack of good antioxidants —Lack of good exercise —Magnesium deficiency —Liver dysfunction (and the use of drugs that impair liver function) —Polluted air —Hypothyroidism —All of these are correctable. When Israel banned food contaminated with xeno-estrogen (pesticides), the incidence of breast cancer dropped over 15 percent within 6 years. We could do the same (and actually much better) for prostate cancer. Given what is already known, it should be possible to reduce the incidence of prostate cancer by 90 percent.
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From about age 40 on, testosterone levels drop at the rate of about one percent per year.
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Because excess testosterone spills over and becomes estrogen, it can cause water retention, breast enlargement, prostate enlargement, atrophy of the genitals, decrease in libido, and cancer. It’s possible that the misconception that testosterone causes prostate cancer has been perpetuated by conventional medicine’s routine use of grossly excessive doses of testosterone and the potent synthetic testosterones.
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It is the balance between progesterone and testosterone with estradiol that is key to the effects of the hormones.
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—The vast majority of early prostate cancer studies used serum levels instead of saliva levels when measuring hormone levels in men (and women). This is a mistake since serum testing does not discriminate between total “free” and protein-bound hormone. It is the “free” hormone that is bio-active, whereas the protein-bound hormone is not bio-active. Thus, serum tests are generally irrelevant since they cannot tell you how much of the “free” hormone is present. This means that the thousands of studies done with serum hormone testing are essentially irrelevant.
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—Since the doubling time of prostate cancer growth is quite slow compared to breast cancer, doctors are often seduced into thinking that their treatments are working when, in fact, such patients, who are generally older men, die from other causes rather than from their cancer.
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—Doctors’ main avenue of learning (besides visiting “reps” from the pharmaceutical industry) is the CME (Continuing Medical Education) seminars. He/she must attend at least 50 hours of accredited CME seminars every three years. He does not know that accreditation is determined by an AMA panel made up of doctors representing pharmaceutical companies, or that virtually all of the speakers represent pharmaceutical companies. The doctor rarely hears of alternative effective treatments. Pharmaceutical-sponsored seminars are often more convenient and low-cost or free, whereas the unaccredited alternative seminars usually require a little travel and there is a cost for attending.
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The ratio of testosterone to estradiol (T/E2) is the major operant factor.
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Thus, the ratio of progesterone to estradiol (the P/E2 ratio) is also very important. Optimal protection against estradiol-induced cancer occurs when the saliva progesterone level is 200 to 300 times that of saliva estradiol level.
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One of the hallmarks of cancer cells is that they will induce angiogenesis that will increase the flow of blood to them. The anti-angiogenesis function of PSA is a defense against abnormally growing cells in the prostate. Firm massage of normal prostate cells will increase PSA levels in the prostate. Thus, PSA is a marker for increased crowding of normal prostate cells.
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As men age, their testosterone and progesterone levels fall. These are the two hormones known to be anabolic—meaning that they produce energy, rather than using up energy, such as estrogen and insulin do. With the fall of testosterone and progesterone, cellular energy wanes. Only the cancer cell, with its ability to create angiogenesis, retains its high energy. When a testosterone-deficient man has his testosterone restored, normal cells then have more energy and, thus, can produce more PSA. This is why PSA tends to rise a bit when testosterone is restored. The PSA is a defense factor and the increased PSA inhibits angiogenesis of the cancer cells. If one’s PSA rises a bit after the testosterone is brought up to normal physiological levels of a younger man, it is not a sign that the cancer is growing, but, instead, is a sign that the normal cells have become stronger in fighting against the cancer cells. Maintaining good levels of both progesterone and testosterone should be the goal of men for preventing, and for treating, prostate cancer.
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Progesterone inhibits 5-alpha-reductase, an enzyme that otherwise would convert testosterone into dihydrotestosterone (DHT) that is thought to cause prostate hypertrophy (enlargement). Progesterone thus helps maintain normal testosterone levels and inhibits production of DHT. Progesterone is also an anabolic (energy-raising) hormone.
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— Testosterone is our most potent anabolic hormone, and thus very important to metabolism throughout the body. Testosterone is also a direct antagonist of estradiol. The balance of testosterone versus estradiol = balance between masculinity and femininity. Maintaining a good T/E2 ratio reduces risk of prostate cancer.
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— Both progesterone and testosterone promote the p53 gene that leads to normal healthy cell apoptosis (normal cell death), important to cancer prevention. Estradiol, on the other hand, promotes the Bcl-2 gene, a known oncogene that inhibits apoptosis and causes cancer. Thus, maintaining the proper ratio of these hormones to estradiol is important in preventing and treating prostate cancer.
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To restore hormone balance we’re looking for: Saliva progesterone levels that are 200 to 300 times that of estradiol or around 400 pg/ml (in a two-ounce jar or tube of cream containing 960 mg of progesterone, this would be a bit less than 1/8 tsp of cream daily). The ratio of saliva testosterone to estradiol should be about 200 to 300 to 1. The saliva testosterone level should be approximately 200 to 300 pg/ml. Creams with the proper testosterone content are not readily available, so ask your doctor to write a prescription for the cream, then take it to a compounding pharmacist. It is essential that the pharmacist use real testosterone, and not one of the synthetic versions such as methyltestosterone. General dosages for men deficient in progesterone and/or testosterone: Transdermal progesterone . . . . . . 5 to 8 mg/day Transdermal testosterone . . . . . . . 1 to 2 mg/day I have seen remarkable benefits and no side effects in men who use hormones this way. The low doses used attest to the excellent absorption of these hormones when applied transdermally (via creams, through the skin). Though retired, I keep in contact with a number of my patients with prostate cancer that I had treated with diet, antioxidants, progesterone and testosterone (as described above) and these men, now 16 years later, remain in good health, without having to resort to surgery or chemotherapy. Dosages for individuals can vary depending on absorption and excretion kinetics. It is wise to re-test saliva levels after 2 to 3 months of transdermal hormone use. When testing for the effect of transdermally applied hormone, it is wise to standardize the time between dosing and the time of saliva collection. I recommend saliva collection be done 10 hours after application of the hormone. In this manner, serial testing will be more informative and reliable.
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DHEA seems to have more benefits and fewer risks for men than women, which may be due to the fact that it converts to either testosterone or estrogen before excretion. In this process, it follows the path of least resistance: it will become testosterone in people with low testosterone, or estrogen in people with low estrogen levels. Thus, the ultimate effects of DHEA supplementation, if any, are difficult to predict.
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The recommended dose of DHEA for men is 10 to 25 mg a day. If you have your DHEA levels checked with a blood test, remember that DHEA-S is the relatively inactive form. Saliva DHEA testing is a more accurate measurement of the active DHEA in the blood.
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In addition to creating hormone balance, it is wise to supplement 20 to 30 mg of zinc daily. Zinc is a potent antioxidant, and an aromatase inhibitor. Zinc levels are especially high in prostate tissue. I also recommend supplementary anti-oxidant vitamins (vitamins C, A, and E), the mineral selenium in doses of 60 to 120 mcg per day, and in older men, vitamin D in doses of 400 mg daily. A number of recent studies have shown that adequate vitamin D levels may help prevent prostate cancer.
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